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Changes of DNA accessibility and RNA transcription upon SWI/SNF inhibition in peripheral blood and bone marrow cells [multiome]

ABSTRACT: Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on peripheral blood (PB) and bone marrow (BM) cells in mice. We identify altered chromatin regulatory mechanisms in B cells and monocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE205570 | GEO | 2023/01/10

REPOSITORIES: GEO

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Transcriptional changes in bone marrow cells upon SWI/SNF inhibition [scRNA-seq]

Project description:Despite significant therapeutic potential of SWI/SNF inhibition therapy, the off-tumor effects of SWI/SNF inhibition remain largely unknown. Here, we quantify the effects of the dual SWI/SNF ATPase inhibitor BRM014 on bone marrow cells in mice. We identify lineage-dependent effects on the B and monocyte lineages within the bone marrow.

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Inhibition of SWI/SNF broadly disrupts enhancers and reveals remodeler redundancy at promoters

Project description:Appropriate gene expression requires the establishment of accessible chromatin at promoters and enhancers. These patterns are maintained thorugh the action of, such as the SWI/SNF family. Despite this critical role, previous studies have remained inconclusive regarding the direct role of SWI/SNF. Herein, we employ BRM014, a fast-acting small-molecule inhibitor of the SWI/SNF ATPase subunit, to probe the direct response of mouse embryonic stem cells to disruption of appropriate SWI/SNF chromatin remodeling activity. We demonstrate that the immediate role of SWI/SNF inhibition is a broad loss of chromatin accessibility at both promoter and enhancer loci, and this is reflected in an associated reduction in nascent transcription. We determine that this initial perturbation can be compensated for at a majority of gene promoters, such that these elements regain accessibilty and gene expression under prolonged treatment. However, a subset of gene promoters, as well as most enhancers, fail to recover under these conditions. Finally, we identify EP400 as a putative factor driving compensation ability, as the loss of this factor impedes promoter recovery.

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SWI/SNF-dependent genes are defined by their chromatin landscape [MNase-seq]

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